Innovating Beyond Cardiology: Discoveries in Acquired Chronic Muscle Spasm and Resulting Chronic Pain

One of the most common ills of mankind is chronic pain. In some cases, the associated chronic muscle spasm is known to be the culprit.  

However, in some cases there is not an obvious connection between the pain and the chronic muscle spasm that was responsible for the chronic pain. In any case, treatment of chronic pain requires knowledge of its source. If chronic muscle spasm is indeed the source, then it is necessary to have a diagnostic tool to identify the muscle or muscles in chronic spasm.  

Ultimately, a treatment that specifically targets chronic muscle spasm is then needed to successfully treat the chronic pain.   

What is not generally known is that muscles in chronic spasm are very electrically active. Use of an EMG device, that is essentially an EKG for muscle, is all that is needed to identify a muscle in chronic spasm. Unlike EKG devices, a needle must be inserted into the muscle to record the electrical activity.  

Surface recordings of EMG are possible but only tell of generalised electrical activity and do not identify specific muscles. When treatment of muscles in chronic spasm involves an injection technique, not only the specific muscle but all segments of the muscle demonstrating enhanced electrical activity need to be identified.  

Successful treatment by injection will result in elimination of the enhanced electrical activity. Medications such as Botox have a slow onset and the results peak at about two weeks. Medication combinations such as Lidocaine/Phenoxybenzamine have an initial immediate effect of resolution of the enhanced electrical activity and a secondary effect that can last for months.  

When Lidocaine is utilised, it is possible to map the entire muscle and verify that all parts of the muscle that demonstrated enhanced electrical activity have been treated and adequately suppressed.   

Getting back to basics, muscles in chronic spasm can cause pain at a distance. One of the most obvious examples is a condition called IT band syndrome which causes knee pain. The muscle that is responsible is the tensor fascia lata, which is a relatively small muscle in the upper anterior thigh.  

Resolution of spasm of that muscle results in near immediate relief of the knee pain. On the other hand, pain resulting from some muscles in chronic spasm results in local pain such as in shin splints that are caused by muscles in the anterior leg below the knee.   

There has been significant controversy regarding the origin of the enhanced electrical activity in various states of muscle activity. However, relative to identification and treatment, the exact origin is of little consequence.  

Prolonged elimination of the enhanced electrical activity, that is identified in the scientific literature as Spontaneous Electrical Activity or SEA, results in resolution of the chronic spasm and sustained relief of chronic pain if it was secondary to the chronic muscle spasm.   

If it can be identified that a muscle is in chronic spasm and appears to be the source of chronic pain, then treatment of the chronic muscle spasm and not suppression of the chronic pain with pain medications such as opioids should be focus of treatment. A treatment protocol named Coletti Method Emg ChemoDenervation (CMECD) has been shown in somewhat limited but statistically significant clinical setting to relieve chronic pain by prolonged suppression of the SEA.  

Fortunately, when this protocol is utilised, the SEA does not return, nor does the muscle spasm or the resulting chronic pain.  

The question remains: how does the muscle go into chronic spasm in the first place?  

What I have postulated is that what is seen in cardiac muscle during a state of contraction is that the contraction of the muscle limits the blood supply that is needed for relaxation of the muscle. It turns out that the muscle needs more blood supply and therefore energy to relax than to contract. It is like a mouse trap, much more effort to set the trap than to set it off.  

Normally, a muscle in spasm does not stay in spasm long enough to limit the energy supply to relax. But if an acquired muscle spasm from an overuse injury is not attended to, then the spasm sets off a chain of events that leads not only to chronic spasm but a degeneration of the muscle with loss of mitochondria and muscle fibers.  

Recovery requires significant time with unimpeded blood supply for new mitochondria to emerge and repair of the muscle fibres. Short-term relief of chronic muscle spasm does not suffice and thus a therapy that has a long-term solution is necessary.  

Alternatively, a therapy performed on a daily basis for months may be sufficient. It is likely that there are a number of therapies that may suffice but will require very frequent applications for at least two-three months depending upon the degree of injury and loss of cellular elements resulting from the prolonged ischemia, ie: poor blood supply.   

I had done research during my cardiology followship that unfortunately was not reported. The findings were that the blood flow during cardiac contraction that is known to be less than during cardiac relaxation can be altered by medications that limit the force of cardiac contraction.  

At a certain point of suppression of cardiac contraction, the predominant cardiac blood supply to the cardiac tissue is predominantly in a state of cardiac contraction. This demonstrates that muscle contraction limits the blood supply.   

Now to the question of the SEA. Where did that come from?  

Let’s first look at the cardiac situation. When there is poor blood supply, we get cardiac arrhythmias. The skeletal muscle is no different. The technical issues are a matter of future research, but the end result is the SEA not only identifies the presence of chronic muscle spasm but is actually the ongoing cause of the chronic spasm. The SEA is like an electrical stimulator, constantly depolarising the skeletal muscle and keeping it in a state of constant contraction, limiting its blood supply and resulting in an unending state of contraction. I call it the black hole of muscle pathophysiology.   

So, what does this newfound knowledge do for us? To start with, it provides us with a method of identifying muscle in true chronic spasm. With that knowledge, we are able to seek alternative treatments to resolve the chronic spasm and we have the means to verify success or failure of those treatments.   

The CMECE procedure is one proven way to treat chronic muscle spasm and resultant chronic pain secondary to chronic muscles spasm. It can be performed by any medical professional that is allowed to do intramuscular injections and has minimal risk. Cost is also relatively minimal with a one-time procedure, all that is necessary, likely to be under $500 for all costs incurred.   

Other procedures should be able to be developed given the understanding of the cause of chronic muscle spasm and may not require injection of any medication. Hopefully, these treatments will emerge. In the meantime, the CMECD procedure is available to be performed worldwide and holds the opportunity to relieve chronic pain in a large portion of those with chronic pain.   

Dr Roger H. Coletti is Medical Director at Fasano Underwriting, a Longevity Holdings company